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首页> 外文期刊>Life sciences >Ganoderma total sterol (GS) and GS(1) protect rat cerebral cortical neurons from hypoxia/reoxygenation injury.
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Ganoderma total sterol (GS) and GS(1) protect rat cerebral cortical neurons from hypoxia/reoxygenation injury.

机译：灵芝总固醇（GS）和GS（1）保护大鼠大脑皮质神经元免受缺氧/复氧损伤。

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摘要

The effect of Ganoderma total sterol (GS) and its main components(GS(1)) on rat cortical neuronal cultures exposed to hypoxia/reoxygenation (H/R) was studied in vitro. GS (0.01,0.1,1 mug/ml) increased neuron viability following H/R. GS also significantly reduced malondialdehyde content and reactive oxygen species production and increased manganese superoxide dismutase (Mn-SOD) activity; furthermore, the translocation of nuclear factor-kappa B and the production of interleukin-1beta and tumor necrosis factor alpha induced by H/R were also blocked. These findings suggest that GS might be useful in treating H/R-induced oxidative stress and inflammatory response. We also hypothesized that Mn-SOD might play a critical role in the neuroprotective effect of GS against H/R injury. In addition, pretreatment with GS(1) (0.01, 0.1, 1 mug/ml) significantly attenuated the decline of neuron viability and the formation of reactive oxygen species. Furthermore GS(1) possessed more potent protective effect on neurons compared with GS at the same dose. These findings demonstrated that GS(1) is the main component in GS; and play a critical role in the neuroprotective effect of GS against H/R.
机译：体外研究了灵芝总固醇（GS）及其主要成分（GS（1））对暴露于缺氧/复氧（H / R）的大鼠皮质神经元培养物的影响。 GS（0.01,0.1,1杯/毫升）在H / R后增加神经元活力。 GS还显着降低了丙二醛含量和活性氧的产生，并增加了锰超氧化物歧化酶（Mn-SOD）的活性;此外，H / R诱导的核因子-κB易位以及白介素-1β和肿瘤坏死因子α的产生也​​被阻断。这些发现表明，GS可能在治疗H / R诱导的氧化应激和炎症反应中有用。我们还假设Mn-SOD可能在GS对H / R损伤的神经保护作用中起关键作用。此外，用GS（1）（0.01、0.1、1杯/毫升）进行的预处理显着减弱了神经元活力的下降和活性氧的形成。此外，与相同剂量的GS相比，GS（1）对神经元具有更强的保护作用。这些发现表明，GS（1）是GS中的主要成分。并在GS对H / R的神经保护作用中起关键作用。

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